Mechanisms of cell membrane damage and degradation during anoxic injury induced in the isolated perfused kidney and isolated renal cells will be examined. Tissue and cells obtained during anoxia or reoxygenation following anoxia will be biochemically analyzed for membrane phospholipid degradation and peroxidation of fatty acids. The release by injured cells of prostaglandins and metabolites of prostacyclin and thomboxane B2 will be studied. Attempts will be made to protect kidneys from anoxic injury by the use of phospholipase inhibitors and membrane stabilizing agents. Mechanisms of calcium cytotoxicity will be analyzed for the possible role played by calcium activated phospholipases. The roles played by molecular charge, antigen valence and antigen-antibody affinity in hapten mediated immune complex glomerulonephritis will be delineated. Methods used will include lipid analysis, prostaglandin radioreceptor and radioimmunoassay, spectrophotometric techniques, light and electron microscopy, equilibrium dialysis, sucrose gradient centrifugation, immunofluorescence, protein modification and affinity chromatography.